Acrylamide exposure induces growth retardation, neurotoxicity, stress, and immune/antioxidant disruption in Nile tilapia (Oreochromis niloticus): The alleviative effects of Chlorella vulgaris diets.

This study looked at the toxic impacts of water-born acrylamide (ACR) on Nile tilapia (Oreochromis niloticus) in terms of behaviors, growth, immune/antioxidant parameters and their regulating genes, biochemical indices, tissue architecture, and resistance to Aeromonas hydrophila. As well as the probable ameliorative effect of Chlorella vulgaris (CV) microalgae as a feed additive against ACR exposure was studied. The 96-h lethal concentration 50 of ACR was investigated and found to be 34.67 mg/L for O. niloticus. For the chronic exposure study, a total of 180 healthy O. niloticus (24.33 ± 0.03 g) were allocated into four groups in tri-replicates (15 fish/replicate), C (control) and ACR groups were fed a basal diet and exposed to 0 and 1/10 of 96-h LC50 of ACR (3.46 mg/L), respectively. ACR+ CV5 and ACR+ CV10 groups were fed basal diets with 5 % and 10 % CV supplements, respectively and exposed to 1/10 of 96-h LC50 of ACR for 60 days. After the exposure trial (60 days) the experimental groups were challenged with A. hydrophila. The findings demonstrated that ACR exposure induced growth retardation (P˂0.01) (lower final body weight, body weight gain, specific growth rate, feed intake, protein efficiency ratio, final body length, and condition factor as well as higher feed conversion ratio). A substantial decrease in the immune/antioxidant parameters (P˂0.05) (lysozyme, serum bactericidal activity %, superoxide dismutase, and reduced glutathione) and neurotransmitter (acetylcholine esterase) (P˂0.01) was noticed with ACR exposure. A substantial increase (P˂0.01) in the serum levels of hepato-renal indicators, lipid peroxidation biomarker, and cortisol was noticed as a result of ACR exposure. ACR exposure resulted in up-regulation (P˂0.05) of the pro-inflammatory cytokines and down-regulation (P˂0.05) of the antioxidant-related gene expression. Furthermore, the hepatic, renal, brain, and splenic tissues were badly affected by ACR exposure. ACR-exposed fish were more sensitive to A. hydrophila infection and recorded the lowest survival rate (P˂0.01). Feeding the ACR-exposed fish with CV diets significantly improved the growth and immune/antioxidant status, as well as modulating the hepatorenal functions, stress, and neurotransmitter level compared to the exposed-non fed fish. In addition, modulation of the pro-inflammatory and antioxidant-related gene expression was noticed by CV supplementation. Dietary CV improved the tissue architecture and increased the resistance to A. hydrophila challenge in the ACR-exposed fish. Noteworthy, the inclusion of 10 % CV produced better results than 5 %. Overall, CV diets could be added as a feed supplement in the O. niloticus diet to boost the fish's health, productivity, and resistance to A. hydrophila challenge during ACR exposure.

Estimating the in vitro cytotoxicity of the newly emerged zinc oxide (ZnO) doped chromium nanoparticles using the human fetal lung fibroblast cells (WI38 cells).

Advances in nanotechnology have been increased for more smart applications and getting the highest level of benefits, recently modification of the surface characters of nanoparticles is a new trend to get the optimal benefits, one of these modification is doping of zinc oxide with chromium nanoparticles (ZnO doped Cr NPs), the present study aimed to identify the surface characters of doped ZnO and their possible cytotoxic effects. The doped NPs were characterized by X-ray diffraction (XRD), Fourier transform infrared (FTIR), Field emission scanning electron microscope (FESEM), and Electromagnetic Data Exchange (EDX). Human fetal lung fibroblast cells (WI38 Cells) was treated with variable concentrations of pure ZnO and ZnO doped Cr (0.01 %, 0.02 %, 0.03 % and 0.04 %) for 24 hr at 37 °C followed by the MTT assay. The cells treated with the obtained half-maximal inhibitory concentration (IC50). The supernatant and cells were collected for oxidant/anti-oxidant and molecular analysis.The observed FESEM features are in line with the reported XRD analysis confirming the hexagonal crystal symmetry of all samples. The findings revealed that pure ZnO exhibited potent cytotoxic effects followed by (0.03 % and 0.04 %). All tested NPs produce lipid peroxidation significantly (0.03 % and 0.04 %). The significant up regulation of Bcl-2-associated X protein (BAX) and apoptotic Caspase (Cas-3) transcription level were reported in ZnO and 0.03 % and 0.04 % in contrast the anti apoptitic B-cell lymphoma 2 (Bcl-2) is elevated in 0.01 % and 0.02 %. Doping of ZnO with Cr causing significant morphological changes which effect on their toxicity especially with 0.03 % and 0.04 %.

Ginger and Propolis Exert Neuroprotective Effects against Monosodium Glutamate-Induced Neurotoxicity in Rats.

Central nervous system cytotoxicity is linked to neurodegenerative disorders. The objective of the study was to investigate whether monosodium glutamate (MSG) neurotoxicity can be reversed by natural products, such as ginger or propolis, in male rats. Four different groups of Wistar rats were utilized in the study. Group A served as a normal control, whereas group B was orally administered with MSG (100 mg/kg body weight, via oral gavage). Two additional groups, C and D, were given MSG as group B along with oral dose (500 mg/kg body weight) of either ginger or propolis (600 mg/kg body weight) once a day for two months. At the end, the rats were sacrificed, and the brain tissue was excised and levels of neurotransmitters, ß-amyloid, and DNA oxidative marker 8-OHdG were estimated in the brain homogenates. Further, formalin-fixed and paraffin-embedded brain sections were used for histopathological evaluation. The results showed that MSG increased lipid peroxidation, nitric oxide, neurotransmitters, and 8-OHdG as well as registered an accumulation of ß-amyloid peptides compared to normal control rats. Moreover, significant depletions of glutathione, superoxide dismutase, and catalase as well as histopathological alterations in the brain tissue of MSG-treated rats were noticed in comparison with the normal control. In contrast, treatment with ginger greatly attenuated the neurotoxic effects of MSG through suppression of 8-OHdG and ß-amyloid accumulation as well as alteration of neurotransmitter levels. Further improvements were also noticed based on histological alterations and reduction of neurodegeneration in the brain tissue. A modest inhibition of the neurodegenerative markers was observed by propolis. The study clearly indicates a neuroprotective effect of ginger and propolis against MSG-induced neurodegenerative disorders and these beneficial effects could be attributed to the polyphenolic compounds present in these natural products.